NDLI: Caspase-8 acts as a molecular rheostat to limit RIPK1- and MyD88-mediated dendritic cell activation.

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Caspase-8 acts as a molecular rheostat to limit RIPK1- and MyD88-mediated dendritic cell activation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Cuda, Carla M. Gierut, Angelica K. Mohan, Chandra Stehlik, Christian Hutcheson, Jack Budinger, G. Scott Hedrick, Stephen M. Misharin, Alexander V. Perlman, Harris Saber, Rana Haines, G. Kenneth
Description	Author Affiliation: Cuda CM ( Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611); Misharin AV ( Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611); Gierut AK ( Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611); Saber R ( Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611); Haines GK ( Department of Pathology, School of Medicine, Yale University, New Haven, CT 06510); Hutcheson J ( Division of Rheumatology, Department of Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390); Hedrick SM ( Division of Biological Sciences, Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093); Mohan C ( Division of Rheumatology, Department of Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390); Budinger GS ( Division of Pulmonary and Critical Care, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611.); Stehlik C ( Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611); Perlman H ( Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611)
Abstract	Caspase-8, an executioner enzyme in the death receptor pathway, was shown to initiate apoptosis and suppress necroptosis. In this study, we identify a novel, cell death-independent role for caspase-8 in dendritic cells (DCs): DC-specific expression of caspase-8 prevents the onset of systemic autoimmunity. Failure to express caspase-8 has no effect on the lifespan of DCs but instead leads to an enhanced intrinsic activation and, subsequently, more mature and autoreactive lymphocytes. Uncontrolled TLR activation in a RIPK1-dependent manner is responsible for the enhanced functionality of caspase-8-deficient DCs, because deletion of the TLR-signaling mediator, MyD88, ameliorates systemic autoimmunity induced by caspase-8 deficiency. Taken together, these data demonstrate that caspase-8 functions in a cell type-specific manner and acts uniquely in DCs to maintain tolerance.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1400122
Journal	The Journal of Immunology
Issue Number	12
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Caspase 8 Immunology Dendritic Cells Immune Tolerance Physiology Myeloid Differentiation Factor 88 Receptor-interacting Protein Serine-threonine Kinases Signal Transduction Animals Autoimmune Diseases Genetics Mice Mice, Knockout Toll-like Receptors Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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